The induction of cleft palates in A/J mice in response to the administration of a glucocorticoid offers an unusual laboratory model for studies on birth defects. Our hypothesis is that the genome is involved, and experiments are proposed to assay for various aspects of the genomic structure and function. The methods call for the isolation of nuclei and cytosol from maxillary processes both from the normal and triamcinolone acetonide (TAC) injected A/J mouse embryos, for the qualitative analysis of soluble cytoplasmic proteins, for the isolation and characterization of poly(A)-messenger RNA, for determining the number of genes affected, and for studies on transcription and the involvement of chromosomal proteins in executing the adverse genetic effects observed in clefting. Our objectives include studies on the distribution of labeled TAC chromatin to ascertain the various binding sites for labeled TAC both in active and inactive genes. Also we have isolated a fraction of chromosomal proteins which appears to be involved in binding to specific gene sequences which may be responsible for cell specialization. We are attempting to find out whether there is a linkage in binding TAC to chromatin and this fraction of chromosomal proteins. Such data will aid in understanding as to how clefting may occur in A/J mice in response to the exposure to teratogens, and may aid in the final analysis as to how teratogens may influence development of the human embryo.